Targeting the podocyte to treat glomerular kidney disease

Lal, Mark; Young, Kenneth W.; Andag, Uwe

doi:10.1016/j.drudis.2015.06.003

Cited by 38 publications

(23 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As terminally differentiated cells, podocytes play a crucial role in establishing the integrity and selective permeability of the glomerular filtration barrier [1–3]. Accumulating evidence has shown that podocyte injury is associated with proteinuria and several glomerular diseases [4–7].…”

Section: Introductionmentioning

confidence: 99%

Dab1 Contributes to Angiotensin II-Induced Apoptosis via p38 Signaling Pathway in Podocytes

Gao

Chen

Zhu

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Numerous studies have found that angiotensin II (Ang II) participates in podocyte apoptosis and exacerbates progression of end-stage kidney disease (ESKD). However, its underlying mechanism remains largely unexplored. As a homolog of Drosophila disabled (Dab) protein, Dab1 plays a vital role in cytoskeleton, neuronal migration, and proliferation. In the present study, our data revealed that Ang II-infused rats developed hypertension, proteinuria, and podocyte injury accompanied by Dab1 phosphorylation and increased reelin expression in kidney. Moreover, Ang II induced podocyte apoptosis in vitro. Dab1 phosphorylation and reelin expression in podocytes were increased after exposure to Ang II. Conversely, Dab1 small interfering RNA (siRNA) exerted protective effects on Ang II-induced podocyte apoptosis, resulting in decreased p38 phosphorylation and reelin expression. These results indicated that Dab1 mediated Ang II-induced podocyte apoptosis via p38 signaling pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Dab1 Contributes to Angiotensin II-Induced Apoptosis via p38 Signaling Pathway in Podocytes

Gao

Chen

Zhu

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…Disruption of the podocyte actin filament is linked to CKD (Reiser and Sever, 2013;Lasagni et al, 2013) and stabilization of the podocyte actin network has been proposed as a therapeutic target (Lal et al, 2015;Tian and Ishibe, 2016). A role for alterations in the podocyte actin cytoskeleton in fibrosis is recently emerging.…”

Section: Glomerular Cellsmentioning

confidence: 98%

The cytoskeleton as a novel target for treatment of renal fibrosis

Parrish

2016

Pharmacology & Therapeutics

View full text Add to dashboard Cite

“…Impairment of the endothelial surface layer leads to albuminuria and vascular disease 123 , and damage to this layer can lead to scarring and glomerulosclerosis 123 . Preclinical and clinical studies have shown that damage to the endothelial surface layer strongly correlates with diabetes-mellitus-induced proteinuria 216,217 .…”

Section: Targeting Renal Cellsmentioning

confidence: 99%

“…Since the discovery of nephrin (encoded by NPHS1 ) and podocin (encoded by NPHS2 ) as integral components of the slit diaphragm, several other podocyte-related proteins, such as glycogen synthase kinase 3b, have been discovered. Mutations in these proteins are linked to genetic diseases of the glomerulus 216 .…”

Section: Targeting Renal Cellsmentioning

confidence: 99%

Nanomedicines for renal disease: current status and future applications

et al. 2016

View full text Add to dashboard Cite

Treatment and management of kidney disease currently presents an enormous global burden, and the application of nanotechnology principles to renal disease therapy, although still at an early stage, has profound transformative potential. The increasing translation of nanomedicines to the clinic, alongside research efforts in tissue regeneration and organ-on-a-chip investigations, are likely to provide novel solutions to treat kidney diseases. Our understanding of renal anatomy and of how the biological and physicochemical properties of nanomedicines (the combination of a nanocarrier and a drug) influence their interactions with renal tissues has improved dramatically. Tailoring of nanomedicines in terms of kidney retention and binding to key membranes and cell populations associated with renal diseases is now possible and greatly enhances their localization, tolerability, and efficacy. This Review outlines nanomedicine characteristics central to improved targeting of renal cells and highlights the prospects, challenges, and opportunities of nanotechnology-mediated therapies for renal diseases.

show abstract

Targeting the podocyte to treat glomerular kidney disease

Cited by 38 publications

References 59 publications

Dab1 Contributes to Angiotensin II-Induced Apoptosis via p38 Signaling Pathway in Podocytes

Dab1 Contributes to Angiotensin II-Induced Apoptosis via p38 Signaling Pathway in Podocytes

The cytoskeleton as a novel target for treatment of renal fibrosis

Nanomedicines for renal disease: current status and future applications

Contact Info

Product

Resources

About